Shorts – "Alzheimer's Disease & Mercury"

Exposure to extremely low levels of mercury produces several of the distinguishing features of Alzheimer's disease (AD). AD, which affects over 4.5 million people in the U.S., is a progressive mental deterioration, characterized by memory loss, confusion, and behavior changes. Neuro-fibrillary tangles and amyloid plaques in brain tissue, found during autopsy, confirm an AD diagnosis.

Studies over the past ten years have found that extremely low levels of mercury produce amyloid plaques and neuro-fibrillary tangles. A 2000 study, performed by G. Olivieri and colleagues, showed that mercury increases the secretion of amyloid protein and causes hyper-phosphorylation of a protein called Tau; both are AD diagnostic markers. In March 2001, researchers at the University of Calgary used digital time-lapse photography to document the production of neuro-fibrillary tangles in snail brain cells. After culturing the cells for 48 hours, the researchers applied a metal chloride solution of mercury, aluminum, lead, cadmium, or manganese to the cells’ growth cones. Only mercury produced the damage that characterizes AD. A video of the experiment “How Mercury Causes Brain Neuron Degeneration is online at http://apollo.ucalgary.ca/mercury/movies/Lor2_QTS_700kb_QD.mov.

Yet another sign of AD is the inhibition of enzymes in the brain. Several studies have found that “mercury inhibits the same enzymes in normal brain tissues as are inhibited in AD brain samples,” according to Boyd E. Haley, Professor and Chair of the Department of Chemistry at the University of Kentucky. Many of these enzymes are thiol sensitive. While mercury is not the only substance that inhibits these enzymes, it is the one that has been consistently elevated in people with Alzheimer's.

Mercury's role as the “smoking gun” in Alzheimer's disease also fits with what is known about the genetics of Alzheimer's. APO-E genotype, which governs a “house-cleaning protein” in the brain, is considered a risk factor for AD. APO-E4 has two arginine sites; APO-E3 has one arginine and one cysteine site; and APO-E2 has two cysteine sites. Cysteine binds to mercury; arginine does not. People who inherited APO-E4 from both parents have no cysteine sites with which to bind and, thereby, inactivate mercury. This group tends to develop Alzheimer's before age 70. The more cysteine sites that a person with APO-E genotype inherits, the later AD develops. People with three mercury-binding sites tend to develop Alzheimer's after age 90. However, the presence or absence of AD in people with APO-E genotype depends upon mercury exposure. As Haley explains, “Genetic susceptibility is involved, but a toxic exposure is required.” He refers to a study of 500 pairs of identical twins. In many cases, only one of the pair developed AD even though they had the same genotype.

Dental Amalgam Mercury Syndrome. New research connects mercury to Alzheimer's disease! (Newsletter) Fall 2000/Winter 2001.

Haley B. Dr. Boyd Haley's rebuttal to the ADA. Available at www.toxicteeth.org. Accessed on March 21, 2007.

Leong CCCW, Syed NI, Lorscheider FL. Retrograde degeneration of neurite membrane structural integrity of nerve growth cones following in vitro exposure to mercury. (Abstract) Neuroreport. 2001;12(4):733-737. Available at www.neurosite.com. Accessed March 21, 2007

Miller DW, Jr. Mercury on the mind. Available at http://lewrockwell.com. Accessed October 12, 2004.

Nash RA. Metals in Medicine. Alternative Therapies. July/August 2005; 11(4):18-24.